Derivation and Validation of a Score for Predicting Poor Neurocognitive Outcomes in Acute Carbon Monoxide Poisoning.

Importance: Preventing neurocognitive sequelae is a major goal of treating acute carbon monoxide (co) poisoning. There is a lack of reliable score systems exist for assessing the probability of these sequelae. Objective: To develop and validate a novel clinical scoring system for predicting poor neurocognitive outcomes after acute co poisoning. Design, Setting, and Participants: This prognostic study included derivation and validation cohorts based on consecutive patient data prospectively collected at university hospitals from January 2006 to July 2021 in Wonju, Republic of Korea, and from August 2016 to June 2020 in Incheon, Republic of Korea. Participants included individuals aged 16 years or older admitted with co poisoning. Data were analyzed from October 2021 to January 2022. Exposures: Clinical and laboratory variables. Main Outcomes and Measures: The outcome of interest was neurocognitive sequelae at 4 weeks after co poisoning. Logistic regression models were used to identify predictors of poor neurocognitive outcomes in the derivation cohort. Outcomes were assessed using the Global Deterioration Scale [GDS] at 1-month after co exposure and classified as good (1-3 points) or poor (4-7 points). Results: A total of 1282 patients (median [IQR] age, 47.0 [35.0-59.0] years; 810 [63.2%] men) were assessed, including 1016 patients in the derivation cohort and 266 patients in the validation cohort. The derivation cohort included 126 patients (12.4%) with poor GDS scores. Among 879 patients in the derivation cohort with 1-year follow-up data, 757 (86.1%) had unchanged GDS scores, 102 (11.6%) had improved GDS scores, and 20 (2.3%) had worsened GDS scores. In the final prediction model, age older than 50 years (1 point), Glasgow Coma Scale score of 12 or less (1 point), shock (1 point), serum creatine kinase level greater than 320 U/L at emergency department presentation (1 point), and no use of hyperbaric oxygen therapy (1 point) remained factors significantly associated with worse outcome; therefore, this scoring system was called COGAS (creatine kinase, hyperbaric oxygen therapy, Glasgow Coma Scale, age, shock). Area under the receiver operating characteristic curve for COGAS score was 0.862 (95% CI, 0.828-0.895) for the derivation cohort and 0.870 (95% CI, 0.779-0.961) for the validation cohort. Conclusions and Relevance: These findings suggest that assessing the COGAS score during the early phase of co poisoning may help identify patients at risk of poor neurocognitive sequelae.

Digital Biomarkers in Living Labs for Vulnerable and Susceptible Individuals: An Integrative Literature Review.

PURPOSE: The study aimed to identify which digital biomarkers are collected and which specific devices are used according to vulnerable and susceptible individual characteristics in a living-lab setting. MATERIALS AND METHODS: A literature search, screening, and appraisal process was implemented using the Web of Science, Pubmed, and Embase databases. The search query included a combination of terms related to "digital biomarkers," "devices that collect digital biomarkers," and "vulnerable and susceptible groups." After the screening and appraisal process, a total of 37 relevant articles were obtained. RESULTS: In elderly people, the main digital biomarkers measured were values related to physical activity. Most of the studies used sensors. The articles targeting children aimed to predict diseases, and most of them used devices that are simple and can induce some interest, such as wearable device-based smart toys. In those who were disabled, digital biomarkers that measured location-based movement for the purpose of diagnosing disabilities were widely used, and most were measured by easy-to-use devices that did not require detailed explanations. In the disadvantaged, digital biomarkers related to health promotion were measured, and various wearable devices, such as smart bands and headbands were used depending on the purpose and target. CONCLUSION: As the digital biomarkers and devices that collect them vary depending on the characteristics of study subjects, researchers should pay attention not only to the purpose of the study but also the characteristics of study subjects when collecting and analyzing digital biomarkers from living labs.

Effect of Hyperbaric Oxygen Therapy Initiation Time in Acute Carbon Monoxide Poisoning.

OBJECTIVES: Hyperbaric oxygen therapy (HBO2) is recommended for symptomatic patients within 24-hour postcarbon monoxide poisoning. Previous studies have reported significantly better outcomes with treatment administered within 6 hours after carbon monoxide poisoning. Thus, we aimed to compare the neurocognitive outcomes according to HBO2 delay intervals. DESIGN: Retrospective analysis of data from our prospectively collected carbon monoxide poisoning registry. SETTING: A single academic medical center in Wonju, Republic of Korea. PATIENTS: We analyzed the data of 706 patients older than 16 years treated with HBO2 with propensity score matching. Based on carbon monoxide exposure-to-HBO2 delay intervals, we classified patients into the early (control, less than or equal to 6 hr) and late (case, 6-24 hr) groups. The late group was further divided into Case-1 (6-12 hr) and Case-2 (12-24 hr) groups. We also compared mild (nonintubated) and severe (intubated) groups. INTERVENTIONS: HBO2. MEASUREMENTS AND MAIN RESULTS: After propensity score matching, Global Deterioration Scale scores at 6 months postcarbon monoxide exposure showed significantly fewer poor outcome patients in the early than in the late group (p = 0.027). The early group had significantly fewer patients with poor outcomes than the Case-2 group (p = 0.035) at 1 month and than the Case-1 (p = 0.033) and Case-2 (p = 0.004) groups at 6 months. There were significantly more patients with poor prognoses at 6 months as treatment interval increased (p = 0.008). In the mild cohort, the early group had significantly fewer patients with poor 6-month outcomes than the late group (p = 0.033). CONCLUSIONS: Patients who received HBO2 within 6 hours of carbon monoxide exposure had a better 6-month neurocognitive prognosis than those treated within 6-24 hours. An increase in the interval to treatment led to an increase in poor outcomes.

Protective effect of a mixture of Aloe vera and Silybum marianum against carbon tetrachloride-induced acute hepatotoxicity and liver fibrosis.

The hepatoprotective effects of ACTIValoe N-931 complex, a mixture of Aloe vera and Silybum marianum, against acute and chronic carbon tetrachloride (CCl(4))-induced liver injuries were investigated. Acute hepatotoxicity was induced by intraperitoneal injection of CCl(4) (50 microl/kg), and ACTIValoe N-931 complex at 85, 170, and 340 mg/kg was administered orally 48, 24, and 2 h before and 6 h after injection of CCl(4). Hepatotoxicity was assessed 24 h after CCl(4) treatment. Liver fibrosis was induced by intraperitoneal injection of CCl(4) for 8 weeks (0.5 ml/kg, twice per week), and mice were treated with ACTIValoe N-931 complex at 85, 170, or 340 mg/kg once a day (p.o.). In both acute hepatotoxicity and liver fibrosis, serum aminotransferase levels and lipid peroxidation were increased and the hepatic glutathione content was decreased. These changes were prevented by ACTIValoe N-931 complex. The ACTIValoe N-931 complex attenuated the increase in tumor necrosis factor-alpha (TNF-alpha), and inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2), mRNA expressions in acute hepatotoxicity. In antifibrotic experiments, tissue inhibitor of metalloprotease-1 (TIMP-1) mRNA expression was attenuated by treatment with ACTIValoe N-931 complex. The ACTIValoe N-931 complex decreased the hepatic hydroxyproline content and the transforming growth factor-beta1 levels. Our results suggest that the ACTIValoe N-931 complex has hepatoprotective effects in both acute and chronic liver injuries induced by CCl(4).

Protective effect of daidzin against D-galactosamine and lipopolysaccharide-induced hepatic failure in mice.

This study examined the effects of daidzin, a major isoflavone from Puerariae Radix, on D-galactosamine (D-GalN) and lipopolysaccharide (LPS)-induced liver failure. Mice were given an intraperitoneal injection of daidzin (25, 50, 100 and 200 mg/kg) 1 h before receiving an injection of D-GalN (700 mg/kg)/LPS (10 microg/kg). Daidzin markedly reduced the elevated serum aminotransferase activity and the levels of lipid peroxidation and tumor necrosis factor-alpha. The glutathione content was lower in the D-GalN/LPS group, which was attenuated by daidzin. The daidzin pretreatment attenuated the swollen mitochondria observed in the d-GalN/LPS group. Daidzin attenuated the apoptosis of hepatocytes, which was confirmed using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling method and a caspase-3 assay. Overall, these results suggest that the liver protection of daidzin is due to reduced oxidative stress and its antiapoptotic activity.